目的探讨甘草酸(glycyrrhizin,GL)抑制肝星状细胞(hepatic stellate cell,HSC)增殖的分子机制。方法采用血小板源生长因子-BB(platelet derived growth factor-BB,PDGF-BB)与GL共同处理肝星状细胞系,MTT与流式细胞术检测细胞周期,定量RT-PCR检测PDGF受体β(PDGFreceptorβ,PDGFRβ)的表达情况;用CCl4处理大鼠,制备肝损伤后肝纤维化模型,分离肝组织进行原代培养,定量RT-PCR检测PDGFRβ的表达情况。结果体外研究表明GL抑制PDGF-BB介导的促HSC增殖作用,同时GL还能够抑制HSC中PDGFRβ的表达;体内研究表明CCl4处理可以上调PDGFRβ的转录水平,而GL可以有效抑制此过程。结论PDGFRβ是GL治疗肝纤维化的作用靶点。
Objective To study the inhibitory mechanism of glycyrrhizin (GL) in the proliferation of hepatic stellate cell (HSC). Methods RB0105 (HSC line) cells were treated with platelet derived growth factor-BB (PEGF-BB) and GL. Their proliferation and call cycle were determined by MTT and flow cytometry, and PDGF receptor β (PDGFRβ) mRNA expression was examined by quantitative RT-PCR. Rat liver fibrosis model was established by CCl4 treatment, and PDGFRβ mRNA expression was alto detected in primary culture of HSC isolated from liver tissue. Results In vitro GL treatment inhibited HSC proliferation mediated by PE)GF-BB and downregulated PDGFRβ mRNA expression in HSC. Moreover, GL treatment also inhibited PDGFRβ mRNA overexpression induced by CCIa exposure. Conclusion PDGFRβ may be the action target of GL in treating liver fibrosis.